1. What, if any, is the difference between a mutation and a substitution?
   
   
2. The size of successive populations is 100, 100000, 200000, and 1000000. What is the "effective population size" (ignoring spatial heterogeneity, mating etc.) ?
   
   
   
3. What is the chance (probability) that a mutation that arose in a single copy and that provides no selective advantage or disadvantage is fixed in population of 500 haploid organisms?
    
4. What is the chance that a mutation that arose in a single copy and that provides no selective advantage or disadvantage is fixed in population of 500 diploid organisms?
   
   
5. What is the relationship between the mutation rate and the substitution rate for selectively neutral mutations?
    
6. Does the same hold true for an advantages mutation?
    
7. You consider mutations that provide no selective advantage or disadvantage.  The mutation rate is assumed to be constant.  You compare two populations of different size over long periods of time. 
   A) The substitution rate in the smaller population would be higher, because the mutations that occur are more easily fixed in the smaller population due to genetic drift.
   B) The substitution rate is approximately the same in the two population. 
   C) The larger population generates more mutations and therefore has higher diversity and a higher substitution rate. 
     
8. A neutral allele is fixed in a population due to random genetic drift.
   The average the time for fixation of a neutral mutation
   A) is shorter in smaller populations.
   B) is independent of population size.
   C) is shorter in larger populations, because the mutation occurs more frequently in the larger population.
    
9. On average it takes 4*N_e generations until a neutral mutation is fixed in a diploid population. An advantages mutation is fixed already after (2/s) ln (2N) generations.
   How many generations will it take a neutral mutation to become fixed in populations of 1000, 10000, 200 000 individuals. How long would it take (according to the formula) for a mutation with a selective advantage of S=0.05 (or 5%)?
     
10. In a population with 200 000 individuals would a mutation with a selective advantage be fixed in a shorter time than a neutral mutation?
     
11. The fixation probability of a single neutral mutation in a population of 10 individuals as compared to a population of 200 000 organisms is
    A) the same, B) higher, C) lower
     
12. The time till fixation for a single neutral mutation in a population of 10 individuals as compared to a population of 200 000 organisms is
    A) the same, B) shorter, C) longer
     
13. What kind of analyses can you perform using clustalx (list at least three items)?
      
14. Which program options and parameters should you adjust in clustalx to obtain a more accurate phylogenetic reconstruction.
      
    
     
15. Assume you have calculated a molecular phylogeny (=tree). Describe at least one approaches that would allow you to assess if a single branch in this tree is significantly supported by the alignment from which this tree was calculated. (Use less than 20 words per approach.)
      
    
16. Briefly d escribe at least three types of methods that are frequently used to calculated trees from aligned sequences.
     
    
     
17. When calculating trees with clustalx/clustalw you have the option to exclude all positions that have a gap in any of the positions from the analyses. The default is to exclude gaps only from the pairwise alignments. Under which conditions might it be advantages to turn on this option, under which conditions might the default setting be preferable?
     
    
    
    
18. 
    
    
    Assume that the tree depicted above was calculated for homologs of enolase. In case an organism's genome encoded more than one homolog these are labeled a and b or 1 and 2 (this is a purely fictional example!).
    
    a) What part of the tree (if any) could be used as an outgroup? (specify what the addressed question would be for the outgroup selected)
    
    b) When did the gene duplication happen that gave rise to homologs a and b in fungi (Yeast and Neurospora).
    
    c) Would we expect to find homologs of a and b in other eukaryotes? If yes, in which groups?
    
    d) What are possible explanation(s) for Plasmodium having paralogs 1 and 2? (extra credit)
    
    
    
19. a) Given the following tree (below), which type of protein appears to be the one labeled as extein? (bet: beta subunit of the F-ATPase, fl: flagellar assembly ATPase, ttf: transcription termination factor.
    
    b) Assuming that the extein sequence was obtained from Burkholderia brasilensis, does this tree give you any reason to suspect that the extein might encode a paralog to the transcription termination factor? (Hint: remember the taxonomy database in Entrez)
    
    c) Does your assessment of potential paralogy change, in case the extein sequence was obtained from Enterobacter cloacae? (assuming that the branching order in the tree below is reliable.)
        Would this change the likely function you assume for this protein?
        Based on this scenario (the one described in your answer to c) would you expect to find more than one ttf in Escherichia.coli?
        In members of the genus Neisseria?
        In Bacillus subtilis?
    
    (If you are an undergraduate student, c is a bonus questions).
    
    

For Graduate students (else extra credit): What could be the reason for purifying selection being much more effective in bacteria than in mammals?

Extra credit: Surprisingly the formula for fixation times [(2/s) ln (2N) generations] allegedly also holds for detrimental mutations. What could be the reason that the avarage time till fixation for a mutation whose carriers have 5% less offsping is the same as the fixation time for a disadvantageous mutation? Or is this just wrong?